Functional neuroimaging of autistic disorders

Rumsey, Judith M.; Ernst, Monique

doi:10.1002/1098-2779(2000)6:3<171::aid-mrdd4>3.0.co;2-n

Cited by 100 publications

(30 citation statements)

References 53 publications

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“…Both autism and schizophrenia are distinguished by abnormal prefrontal cortical activation and difficulty engaging appropriate emotional responses to the external world (Weinberger and Berman, 1996;Rumsey and Ernst, 2000). It will be of interest to see whether these alterations in a 4 b 2 nAChRs contribute to these abnormalities.…”

Section: Discussionmentioning

confidence: 99%

Nicotine Induces Glutamate Release from Thalamocortical Terminals in Prefrontal Cortex

Lambe

Picciotto

Aghajanian

2003

Neuropsychopharmacol

251

216

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It has been proposed that activation of nicotinic acetylcholine receptors (nAChRs) can activate the prefrontal cortex, enhancing attention and cognition. Nicotine can stimulate the release of several different neurotransmitters in many brain regions. In the present study, we found that stimulation of nAChRs by nicotine or the endogenous agonist, acetylcholine (ACh), induces a large spontaneous increase in glutamate release onto layer V pyramidal neurons of the prefrontal cortex. This release of glutamate, measured by spontaneous excitatory postsynaptic currents (sEPSCs) in the prefrontal cortical slice, depends on intact thalamocortical terminals. It can be suppressed by m-opioids or eliminated by blocking action potentials. The increase in sEPSCs is sensitive to low concentrations of nicotine, suggesting the involvement of high-affinity (eg a 4 b 2 ) nAChRs. Recent work has shown alterations in prefrontal a 4 b 2 nAChRs in autism and schizophrenia, two conditions that are distinguished by abnormal prefrontal cortical activation as well as difficulty in certain aspects of cognition and integrating social and emotional cues. We show that mice lacking the b 2 nAChR subunit do not show increased sEPSCs with either nicotine or ACh, again implicating high-affinity nicotinic receptors. These findings give new insight into the mechanism by which nicotine affects excitatory neurotransmission to the output neurons of the cerebral cortex in a pathway that is critical for cognitive function and reward expectation.

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Section: Discussionmentioning

confidence: 99%

Nicotine Induces Glutamate Release from Thalamocortical Terminals in Prefrontal Cortex

Lambe

Picciotto

Aghajanian

2003

Neuropsychopharmacol

251

216

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“…Little reliable evidence has accumulated so far for disorders such as autism (344), whereas developmental dyslexia, a specific impairment of visual and phonological processes affecting ϳ5% of children, has yielded a substantial set of results in the past few years (e.g., Refs. 165, 363, 389; for a review, see Refs.…”

Section: Developmental Disorders: the Case Of Developmental Dyslexiamentioning

confidence: 99%

Renewal of the Neurophysiology of Language: Functional Neuroimaging

Démonet¹,

Thierry²,

Cardebat³

2005

Physiological Reviews

371

207

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Functional neuroimaging methods have reached maturity. It is now possible to start to build the foundations of a physiology of language. The remarkable number of neuroimaging studies performed so far illustrates the potential of this approach, which complements the classical knowledge accumulated on aphasia. Here we attempt to characterize the impact of the functional neuroimaging revolution on our understanding of language. Although today considered as neuroimaging techniques, we refer less to electroencephalography and magnetoencephalography studies than to positron emission tomography and functional magnetic resonance imaging studies, which deal more directly with the question of localization and functional neuroanatomy. This review is structured in three parts. 1) Because of their rapid evolution, we address technical and methodological issues to provide an overview of current procedures and sketch out future perspectives. 2) We review a set of significant results acquired in normal adults (the core of functional imaging studies) to provide an overview of language mechanisms in the “standard” brain. Single-word processing is considered in relation to input modalities (visual and auditory input), output modalities (speech and written output), and the involvement of “central” semantic processes before sentence processing and nonstandard language (illiteracy, multilingualism, and sensory deficits) are addressed. 3) We address the influence of plasticity on physiological functions in relation to its main contexts of appearance, i.e., development and brain lesions, to show how functional imaging can allow fine-grained approaches to adaptation, the fundamental property of the brain. In closing, we consider future developments for language research using functional imaging.

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“…Asperger Syndrome is also associated with later diagnosis than autism and near average or higher intelligence. Those diagnosed with Asperger Syndrome do not show developmental language delay and can be differentiated from autistic disorder in this manner (Rumsey and Ernst 2000). In addition, we are unaware of any fMRI study in which either the hidden or embedded figures tasks were used to evaluate brain function in children with ADHD.…”

Section: Introductionmentioning

confidence: 99%